title: L-carnitine treatment partially restores urinary bladder function of streptozotocin diabetic rats.
abstract: BACKGROUND
  Diabetes mellitus is associated with urinary bladder dysfunction. This study determined whether or not detrusor responses were altered and reversed by L-carnitine treatment in the urinary bladders of diabetic rats.
  
  
  METHODS
  Three groups of animals were used: streptozotocin-treated (45 mg x kg(-1) i.p., 8 weeks), parallel L-carnitine-treated (0.6 g x kg(-1) x day(-1) i.p.), and control rats. Contractile and relaxant responses were measured using isolated bath techniques.
  
  
  RESULTS
  Serum glucose levels in diabetic rats were partially reversed after L-carnitine treatment. Detrusor strips from diabetic rats exhibited an increase in response to electrical field stimulation (EFS; 0.5-32 Hz). Treatment with L-carnitine restored the hyperreactivity to EFS-induced contractility. The response to direct activation of the smooth muscle with carbachol and KCl remained unaltered. In relaxation studies, the urinary bladders of diabetic rats displayed a diminished response to isoprenaline, an unchanged response to ATP, and an increased response to adenosine of the ATP metabolite. L-carnitine treatment restored the hyporesponsiveness of isoprenaline and the hyperresponsiveness of adenosine-elicited relaxation.
  
  
  CONCLUSIONS
  These findings show that carnitine can be implicated in the contractile response of noradrenergic noncholinergic nerve stimulation and the relaxation response of isoprenaline and adenosine. Hence, L-carnitine deficiency can contribute to voiding deficiency in diabetic patients.
authors.affiliation: Department of Pharmacology, School of Pharmacy, Ankara University, Ankara, Turkey. sgur@pharmacy.ankara.edu.tr
authors.forename: Serap
authors.initials: S
authors.lastname: Gur
authors.forename: Ali Murat
authors.initials: AM
authors.lastname: Irat
mesh_terms: D000241:Adenosine / Q000378:metabolism; D000255:Adenosine Triphosphate / Q000378:metabolism; D000318:Adrenergic beta-Agonists / Q000494:pharmacology; D000818:Animals; D001341:Autonomic Nervous System / Q000187:drug effects* / Q000503:physiopathology; D001786:Blood Glucose / Q000187:drug effects; D002217:Carbachol / Q000494:pharmacology; D002331:Carnitine / Q000494:pharmacology*; D018679:Cholinergic Agonists / Q000494:pharmacology; D003921:Diabetes Mellitus, Experimental / Q000150:complications* / Q000188:drug therapy / Q000503:physiopathology; D004305:Dose-Response Relationship, Drug; D004558:Electric Stimulation; D007545:Isoproterenol / Q000494:pharmacology; D008297:Male; D009119:Muscle Contraction / Q000187:drug effects*; D009126:Muscle Relaxation / Q000187:drug effects*; D051381:Rats; D001743:Urinary Bladder / Q000187:drug effects* / Q000294:innervation / Q000503:physiopathology; D053201:Urinary Bladder, Overactive / Q000188:drug therapy* / Q000209:etiology / Q000503:physiopathology
chemical_list: D000318:Adrenergic beta-Agonists; D001786:Blood Glucose; D018679:Cholinergic Agonists; D000255:Adenosine Triphosphate; D002217:Carbachol; D000241:Adenosine; D007545:Isoproterenol; D002331:Carnitine